转录激活缺陷型c-MycS保留调节增殖和凋亡的能力。
Transactivation-defective c-MycS retains the ability to regulate proliferation and apoptosis.
作者信息
Xiao Q, Claassen G, Shi J, Adachi S, Sedivy J, Hann S R
机构信息
Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2175 USA.
出版信息
Genes Dev. 1998 Dec 15;12(24):3803-8. doi: 10.1101/gad.12.24.3803.
Abstract
Transcriptional activation by c-Myc through specific E box elements is thought to be essential for its biological role. However, c-MycS is unable to activate transcription through these elements and yet retains the ability to stimulate proliferation, induce anchorage-independent growth, and induce apoptosis. In addition, c-MycS retains the ability to repress transcription of several specific promoters. Furthermore, c-MycS can rescue the c-myc null phenotype in fibroblasts with homozygous deletion of c-myc. Taken together, our data argue against the paradigm that all of the biological functions of c-Myc are mediated by transcriptional activation of specific target genes through E box elements.
摘要
c-Myc通过特定E盒元件进行的转录激活被认为对其生物学作用至关重要。然而，c-MycS无法通过这些元件激活转录，但仍保留刺激增殖、诱导不依赖贴壁生长和诱导凋亡的能力。此外，c-MycS保留了抑制几个特定启动子转录的能力。此外，c-MycS可以挽救c-myc纯合缺失的成纤维细胞中的c-myc无效表型。综上所述，我们的数据与c-Myc的所有生物学功能都是通过E盒元件对特定靶基因的转录激活来介导的这一范式相悖。
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